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内体性突触小泡生物发生所需的AP-3复合物与一种酪蛋白激酶Iα样亚型相关。

The AP-3 complex required for endosomal synaptic vesicle biogenesis is associated with a casein kinase Ialpha-like isoform.

作者信息

Faundez V V, Kelly R B

机构信息

Department of Biochemistry and Biophysics, Hormone Research Institute, University of California, San Francisco 94143-0534, USA.

出版信息

Mol Biol Cell. 2000 Aug;11(8):2591-604. doi: 10.1091/mbc.11.8.2591.

Abstract

The formation of small vesicles is mediated by cytoplasmic coats the assembly of which is regulated by the activity of GTPases, kinases, and phosphatases. A heterotetrameric AP-3 adaptor complex has been implicated in the formation of synaptic vesicles from PC12 endosomes (). When the small GTPase ARF1 is prevented from hydrolyzing GTP, we can reconstitute AP-3 recruitment to synaptic vesicle membranes in an assembly reaction that requires temperatures above 15 degrees C and the presence of ATP suggesting that an enzymatic step is involved in the coat assembly. We have now found an enzymatic reaction, the phosphorylation of the AP-3 adaptor complex, that is linked with synaptic vesicle coating. Phosphorylation occurs in the beta3 subunit of the complex by a kinase similar to casein kinase 1alpha. The kinase copurifies with neuronal-specific AP-3. In vitro, purified casein kinase I selectively phosphorylates the beta3A and beta3B subunit at its hinge domain. Inhibiting the kinase hinders the recruitment of AP-3 to synaptic vesicles. The same inhibitors that prevent coat assembly in vitro also inhibit the formation of synaptic vesicles in PC12 cells. The data suggest, therefore, that the mechanism of AP-3-mediated vesiculation from neuroendocrine endosomes requires the phosphorylation of the adaptor complex at a step during or after AP-3 recruitment to membranes.

摘要

小囊泡的形成由细胞质衣被介导,衣被的组装受GTP酶、激酶和磷酸酶活性的调节。一种异源四聚体AP-3衔接蛋白复合体与从PC12内体形成突触小泡有关()。当小GTP酶ARF1被阻止水解GTP时,我们可以在一个组装反应中重组AP-3募集到突触小泡膜上,该反应需要高于15摄氏度的温度和ATP的存在,这表明衣被组装涉及一个酶促步骤。我们现在发现了一种酶促反应,即AP-3衔接蛋白复合体的磷酸化,它与突触小泡衣被有关。磷酸化发生在复合体的β3亚基上,由一种类似于酪蛋白激酶1α的激酶催化。该激酶与神经元特异性AP-3共同纯化。在体外,纯化的酪蛋白激酶I在其铰链结构域选择性地磷酸化β3A和β3B亚基。抑制该激酶会阻碍AP-3募集到突触小泡。在体外阻止衣被组装的相同抑制剂也会抑制PC12细胞中突触小泡的形成。因此,数据表明,AP-3介导的神经内分泌内体囊泡化机制在AP-3募集到膜的过程中或之后的某个步骤需要衔接蛋白复合体的磷酸化。

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